The Effects of Smoking on Memory Consolidation

Mangan, G. L.; Golding, J.F.

doi:10.1080/00223980.1983.9923599

Cited by 34 publications

(29 citation statements)

References 21 publications

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“…Importantly, the number that were recalled from the first block was greater when nicotine was taken after the input of the information, which confirms the findings of Mangan and Golding (1983) and Colrain et al (1992) with paired associate learning in people and a number of associative learning studies with animals (Garg and Holland 1968;Garg 1969;Bfittig 1970;Evangelista et al 1970;Erickson 1971) showing that post-trial nicotine can facilitate memory. The improvement with postlearning dosing shows that nicotine can have a direct effect on memory storage processes.…”

Section: Discussionsupporting

confidence: 84%

“…1970;Erickson 1971). Similarly, in human studies, Mangan and Golding (1983) found that smoking a single cigarette immediately after acquisition of a paired-associate learning task produced superior recall after i month and, more recently, Colrain and colleagues (Colrain et al 1992) found further evidence that post-learning smoking improved memory consolidation in a paired-associate learning task.…”

Section: Tested the Effects Of Smokingmentioning

confidence: 95%

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A comparison of the attentional and consolidation hypotheses for the facilitation of memory by nicotine

1992

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Studies examining facilitation of human memory by the administration of nicotine have given equivocal results and it has been argued that the positive findings on memory may have resulted indirectly from an effect on attention, rather than from a direct effect on memory storage. This study compared the "attentional" and the "mnemonic" hypotheses directly, by using both immediate and delayed recall tasks in a verbal free recall study, in which volunteers smoked on a fixed regime during presentation of a 32 word list (namely, one puff after each of eight 4-word blocks). The serial position curve for immediate recall demonstrated a significant improvement on the later blocks of the list (an attentional effect) when volunteers smoked a nicotine-containing cigarette. However, improved performance was found for items at the beginning of the list on the delayed recall measure and this improvement was significant on the first block of 4 words. Since nicotine input had been taken after presentation of this information, the results demonstrate post-learning facilitation of memory by nicotine.

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Section: Discussionsupporting

confidence: 84%

Section: Tested the Effects Of Smokingmentioning

confidence: 95%

A comparison of the attentional and consolidation hypotheses for the facilitation of memory by nicotine

1992

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“…Since associative processing is necessary to extract meaning from text, the validity of their conclusions must also be considered in respect of the positive effects of nicotine reported in studies directly concerned with associative components of the memory trace. Mangan and colleagues [18,19] have repeatedly demonstrated positive effects of pre-administration of nicotine on paired associative learning for lists with high intralist similarity.…”

Section: Evidence From Cholinergic Agonistsmentioning

confidence: 99%

“…We have also developed the attention hypothesis as an explanation of the intriguing work involving post-learning administration of nicotine; animal studies [20] and some human studies [19,21] have reported facilitation by nico tine on memory tasks when nicotine is administered AFTER the to-be-remembered material.…”

Section: Evidence From Cholinergic Agonistsmentioning

confidence: 99%

Cholinergic Control of Cognitive Resources

Warburton¹,

Rusted

1993

Neuropsychobiology

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In this paper, we describe our approach to the investigation of cholinergic modulation of human information processing. In a continuing series of studies from our laboratories, we have systematically examined the extent to which current psychological models of information processing provide an adequate framework for the interpretation of the modulatory effects of cholinergic agents on cognitive performance measures. We suggest that the data are consistent with the view of attention and memory as processes which operate through a common, limited capacity executive mechanism, rather than separable serial processes described in the traditional modular models of memory.

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“…In addition to its rewarding effects, acute nicotine has cognitive enhancing properties in humans. Specifically, acute nicotine administration enhances attention (Parrott and Craig 1992;Bates et al 1995;Hahn et al 2007;Hong et al 2011), learning and memory (Mangan and Golding 1983;Peeke and Peeke 1984;Warburton et al 1986;Colrain et al 1992), and information processing (Wesnes and Warburton 1983;Provost and Woodward 1991;for review, see Sherwood 1993). In agreement with human studies, there is a great body of evidence suggesting that acute nicotine augments hippocampus-dependent contextual and spatial learning and memory while not affecting hippocampus-independent subtypes of learning (e.g., cued learning) in rodents.…”

Section: Nicotinementioning

confidence: 99%

Effects of drugs of abuse on hippocampal plasticity and hippocampus-dependent learning and memory: contributions to development and maintenance of addiction

2016

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It has long been hypothesized that conditioning mechanisms play major roles in addiction. Specifically, the associations between rewarding properties of drugs of abuse and the drug context can contribute to future use and facilitate the transition from initial drug use into drug dependency. On the other hand, the self-medication hypothesis of drug abuse suggests that negative consequences of drug withdrawal result in relapse to drug use as an attempt to alleviate the negative symptoms. In this review, we explored these hypotheses and the involvement of the hippocampus in the development and maintenance of addiction to widely abused drugs such as cocaine, amphetamine, nicotine, alcohol, opiates, and cannabis. Studies suggest that initial exposure to stimulants (i.e., cocaine, nicotine, and amphetamine) and alcohol may enhance hippocampal function and, therefore, the formation of augmented drug-context associations that contribute to the development of addiction. In line with the self-medication hypothesis, withdrawal from stimulants, ethanol, and cannabis results in hippocampus-dependent learning and memory deficits, which suggest that an attempt to alleviate these deficits may contribute to relapse to drug use and maintenance of addiction. Interestingly, opiate withdrawal leads to enhancement of hippocampus-dependent learning and memory. Given that a conditioned aversion to drug context develops during opiate withdrawal, the cognitive enhancement in this case may result in the formation of an augmented association between withdrawalinduced aversion and withdrawal context. Therefore, individuals with opiate addiction may return to opiate use to avoid aversive symptoms triggered by the withdrawal context. Overall, the systematic examination of the role of the hippocampus in drug addiction may help to formulate a better understanding of addiction and underlying neural substrates.Addiction is a major worldwide health problem that results in maladaptive behavioral changes, some that can last a lifetime. This behavioral plasticity, often times maladaptive, must be associated changes in neural plasticity. In fact, it has been noted multiple times that there is a high degree of overlap between the neurobiology of learning and memory and the neurobiology of addiction

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The Effects of Smoking on Memory Consolidation

Cited by 34 publications

References 21 publications

A comparison of the attentional and consolidation hypotheses for the facilitation of memory by nicotine

A comparison of the attentional and consolidation hypotheses for the facilitation of memory by nicotine

Cholinergic Control of Cognitive Resources

Effects of drugs of abuse on hippocampal plasticity and hippocampus-dependent learning and memory: contributions to development and maintenance of addiction

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